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Background Mechanism(s) connecting obstructive sleep apnoea syndrome (OSAS) to liver injury in paediatric non-alcoholic fatty liver disease (NAFLD) are unknown. We hypothesised alterations in gut-liver axis and in the pool and phenotype of hepatic progenitor cells (HPCs) may be involved in OSAS-associated liver injury in NAFLD. Methods Eighty biopsy-proven NAFLD children (age, mean±SD, 11.4±2.0 years, 56% males, body mass index z-score 1.95±0.57) underwent a clinical- biochemical assessment, with measurement of insulin sensitivity, plasma cytokines, lipopolysaccharide (LPS), an intestinal permeability test and a standard polysomnography. Hepatic toll-like receptor (TLR)-4 expression by liver-resident cells and overall number and expression of resistin and adiponectin by HPCs were assessed by immunofluorescence and immunohistochemistry. OSAS was defined by an apnoea/ hypopnoea index =1. Results OSAS was characterised by an increased intestinal permeability and endotoxemia, coupled with TLR-4 upregulation in hepatocytes, Kupffer and hepatic stellate cells (HSCs) and by an expansion of an adiponectin-deficient HPC pool, key features of steatohepatitis and fibrosis. The duration of haemoglobin desaturation (SaO2 <90%) independently predicted intestinal permeability (ß: 0.396; p=0.026), plasma LPS (ß: 0.358; p=0.008) and TLR-4 expression by hepatocytes (ß: 0.332; p=0.009), Kupffer cells (ß: 0.357; p=0.006) and HSCs (ß:0.445; p=0.002). SaO2 <90% predicted also HPC number (ß: 0.471; p=0.001) and impaired adiponectin expression by HPC pool (ß: -0.532; p=0.0009). These relationships were observed in obese and nonobese children. Conclusions In paediatric NAFLD, OSAS is associated with increased endotoxemia coupled with impaired gut barrier function, with increased TLR-4-mediated hepatic susceptibility to endotoxemia and with an expansion of an adiponectin-deficient HPC pool. These alterations may represent a novel pathogenic link and a potential therapeutic target for OSAS-associated liver injury in NAFLD. [ABSTRACT FROM AUTHOR]

Objective: To investigate whether dietary supplementation with docosahexaenoic acid (DHA) decreases liver fat content in children with non-alcoholic fatty liver disease (NAFLD). Design, Setting and Patients: We performed a randomised controlled trial of DHA supplementation (250 and 500 mg/day) versus placebo in 60 children with biopsy-proven NAFLD (20 children per group). Main Outcome Measures: The main outcome was the change in liver fat content as detected by ultrasonography after 6 months of treatment. Secondary outcomes were the changes in insulin sensitivity index, alanine transaminase, triglycerides and body mass index after 6 months of treatment. Results: Blood DHA increased in children supplemented with DHA (0.65%, 95% CI 0.30% to 1.10% for the DHA 250 mg group and 1.15%, 0.87% to 1.43% for the DHA 500 mg group). The odds of more severe versus less severe liver steatosis after treatment was lower in children treated with DHA 250 mg/day (OR = 0.01, 0.002 to 0.11, p <0.001) and DHA 500 mg/day (OR = 0.04, 0.002 to 0.46, p = 0.01) as compared to placebo but there was no difference between the DHA groups (p = 0.4). Insulin sensitivity index increased and triglycerides decreased to a similar degree in both DHA groups as compared to placebo but there was no effect on alanine transaminase and body mass index. Conclusion: DHA supplementation improves liver steatosis and insulin sensitivity in children with NAFLD. [ABSTRACT FROM AUTHOR]

The article discusses the non-alcoholic fatty liver disease (NAFLD) in children. It mentions that NAFLD has become the common liver disease in children as well as adolescents due to overweight and obesity during their childhood. It states that NAFLD is associated with type 2 diabetes mellitus. It adds that NAFLD causes insulin resistance.

In this article, the author offers views on the treatment of Vitamin D and liver fibrosis. He mentions that liver fibrosis is a reversible wound-healing response caused by the hepatic stellate cell (HSC)-mediated excessive accumulation of extracellular matrix proteins. He also mentions that demonstration of the antifibrotic effect of Vitamin D in liver fibrosis providing additional support to previous pivotal studies.

This article discusses the difficulties in predicting the hepatitis C virus' (HCV) course progression. HCV, particularly in comorbid male adults over 40, can lead to the progression of fibrosis and the development of cirrhosis. Alcohol consumption also greatly increases the risk of cirrhosis. Different studies however, have shown that ethnicity may also increase the risk of cirrhosis in HCV patients. Asian patients had a much higher rate of cirrhosis than white patients, but the study showed that most patients with prolonged HCV will eventually develop cirrhosis. Because of a wide range of results in testing HCV patients, course prediction of the virus is inadequately understood, and prevention of the virus through decreasing the reuse of syringes is still the main objective.